{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T20:02:15Z","timestamp":1791576135891,"version":"4.3.4"},"reference-count":47,"publisher":"National Academy of Sciences","issue":"28","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2012,7,10]]},"abstract":"<jats:p>\n                    The immune response is normally controlled by regulatory T cells (Tregs). However, Treg deficits are found in autoimmune diseases, and therefore the induction of functional Tregs is considered a potential therapeutic approach for autoimmune disorders. The activation of the ligand-activated transcription factor aryl hydrocarbon receptor by 2-(1\u2032\n                    <jats:italic>H<\/jats:italic>\n                    -indole-3\u2032-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) or other ligands induces dendritic cells (DCs) that promote FoxP3\n                    <jats:sup>+<\/jats:sup>\n                    Treg differentiation. Here we report the use of nanoparticles (NPs) to coadminister ITE and a T-cell epitope from myelin oligodendrocyte glycoprotein (MOG)\n                    <jats:sub>35<\/jats:sub>\n                    <jats:sub>\u201355<\/jats:sub>\n                    to promote the generation of Tregs by DCs. NP-treated DCs displayed a tolerogenic phenotype and promoted the differentiation of Tregs in vitro. Moreover, NPs carrying ITE and MOG\n                    <jats:sub>35\u201355<\/jats:sub>\n                    expanded the FoxP3\n                    <jats:sup>+<\/jats:sup>\n                    Treg compartment and suppressed the development of experimental autoimmune encephalomyelitis, an experimental model of multiple sclerosis. Thus, NPs are potential new tools to induce functional Tregs in autoimmune disorders.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1120611109","type":"journal-article","created":{"date-parts":[[2012,6,28]],"date-time":"2012-06-28T20:19:10Z","timestamp":1340914750000},"page":"11270-11275","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":287,"title":["Nanoparticle-mediated codelivery of myelin antigen and a tolerogenic small molecule suppresses experimental autoimmune encephalomyelitis"],"prefix":"10.1073","volume":"109","author":[{"given":"Ada","family":"Yeste","sequence":"first","affiliation":[{"name":"Center for Neurologic Diseases, Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meghan","family":"Nadeau","sequence":"additional","affiliation":[{"name":"Center for Neurologic Diseases, Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Evan J.","family":"Burns","sequence":"additional","affiliation":[{"name":"Center for Neurologic Diseases, Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Howard L.","family":"Weiner","sequence":"additional","affiliation":[{"name":"Center for Neurologic Diseases, Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francisco J.","family":"Quintana","sequence":"additional","affiliation":[{"name":"Center for Neurologic Diseases, Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, MA 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